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X Clin Med Exam 3 > RA, OA and others > Flashcards

RA, OA and others Flashcards

1
Q

What is rheumatoid arthritis?

A 
Autoimmune disease (chronic, systemic, inflammatory disorder affecting whole body and not just joints)
Primarily synovial joints tho
Has extraarticular manifestations
More women (35-50 YO)
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2
Q

Etiology of rheumatoid arthritis

A

Interaction betwwen genes (HLA) and environment

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3
Q

Progression of RA

A

External trigger causing autoimmune rxn and inflammatory process
Synovial hypetrophy and chronic joint inflammation
Destruction of joints (bones and cartilage are eroded)
Joint deformity

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4
Q

Clinical features of RA

A

Symmetrical polyarthritis
Progresses from periphery to more proximal
Usually spare axial skeleton (except C1/2)
Gradual onset with difficulty performing ADLs
May have constitutional features

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5
Q

Predominant sxs of RA

A

Pain, stiffness and swelling of mostly small joints of hands, wrists and forefoot (can be elbows, shoulders, ankles and knees)
Morning stiffness OVER 1 HOUR (gets better with movement)

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6
Q

What is spared in RA?

A

DIP joints

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7
Q

Physical findings in RA

A

TTP or movement of joint
Squeeze tenderness of MCP and MTP joints
Palpable synovial thickening (boggy)
Effusion (fluctuance)

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8
Q

What do the hands look like in RA?

A

Symmetrical inflammation of MCP and PIP
Flexor tendon tenosynovitis (decreased ROM/grip strength, trigger finger)
Swan neck and boutonniere deformities
Ulnar deviation/drift

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9
Q

What do the wrists look like in RA?

A

Loss of extension

Carpal tunnel syndrome (entrapment of nerve due to inflammation)

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10
Q

What do the elbows look like in RA?

A

Loss of extension
Ulnar nerve compression
Rheumatoid nodules most common here

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11
Q

What do the shoulders look like in RA?

A

Seen late in disease (because disease moves distal to proximal)
Frozen shoulder

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12
Q

What do the LEs look like in RA?

A

Feet/ankles: callus formation, hallux valgus (bunion), hammer toes, compensated flexion
Knees: effusion, limited ROM (flexion), Baker’s cyst
Hips: in longstanding disease there is restriction of movement

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13
Q

When is the cervical spine affected in RA?

A

Atlantoaxial joint instability (C1/2) due to chronic inflammation
Cervical subluxation causes neck pain, stiffness and radicular pain (radiating numbness/tingling associated with spinal nerves) that can lead to cervical myelopathy (pinch spinal cord)

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14
Q

What is the significance of extraarticular manifestations in RA?

A

Marker of disease severity (associated with increased morbidity and premature mortality)
Pts more likely to see this: hx of smoking, early onset of physical disability, test + for serum RF

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15
Q

Where can you see extraarticular manifestations in RA?

A

Skin (subcutaneous nodules), eye, pulmonary, cardiovascular (CAD), MSK, hematologic (anemia), CNS (aseptic meningitis)

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16
Q

Felty syndrome

A

Triad of RA, splenomegaly and neutropenia

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17
Q

What is seen in radiography for RA?

A

Preferred INITIAL imaging study

Soft tissue swelling around joint, periarticular osteopenia, joint space narrowing, bony erosions, subluxation

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18
Q

What is the use of MRI and US in RA?

A

More sensitive at detecting changes resulting from synovitis

MRI is valuable for assessing cervical spine

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19
Q

What lab studies do you do for RA?

A

RF, anti-cyclic citrullinated peptide antibodies, ANA (30%), CBC, ESR/CRP, synovial fluid analysis

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20
Q

What is RF?

A

First autoantibody associated with RA
Seen in 75-80% of RA pts (some point in disease)
Moderate specificity
Prognostic value

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21
Q

What are anti-CCP antibodies?

A

Autoantibody most specific for RA
Present in 60-70% pts
Specificity for RA is high
Correlate strongly with erosive disease

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22
Q

CBC in RA

A

See anemia of any chronic disease, thrombocytosis or mild leukocytosis (indicative of an inflammatory process)

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23
Q

Why would ESR/CRP be elevated in RA?

A

Parallels the activity of the disease so it would be high in an active flare

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24
Q

Why is an arthrocentesis used in RA?

A

Diagnosis of exclusion of gout, psuedogout or infection

Synovial fluid analysis can reveal an inflammatory effusion

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25
Q

Who should be tested for RA?

A

People who have at least 1 joint with definite clinical synovitis and they have synovitis that is not better explained by another disease

26
Q

What is seronegative RA?

A

When people lack both RF and anti-CCP antibodies
Can be diagnosed upon findings characteristic of RA if everything else is excluded
Refer to rheum

27
Q

Main goals of RA tx

A

Early DMARDs, treat-to-target strategy to get remission of low disease activity, prevent joint injury, maintain muscle strength and joint mobility

28
Q

Most important non-pharmacoloigc tx or RA

A

Smoking cessation

29
Q

Pharmacologic tx of RA

A

Antiinflammatory agents to control pain and inflammation used in conjunction with DMARDs (disease modifying antirheumatic drugs)

30
Q

What are DMARDs?

A

Slow/halt disease progression to preserve joint function

Start early

31
Q

What is the pretreatment evaluation for before you can use DMARDs?

A

Baseline serology (CBC, creatinine, ESR/CRP, hep b or c)
Ophthalmologic screening for hydroxychloroquine use
TB test
Vaccines

32
Q

Types of DMARDs

A

Nonbiologic (methotrexate)

Biologic (TNF inhibitors etc)

33
Q

Prevalence of osteoarthritis

A

Increases over 50

More women over 55

34
Q

Primary sx of OA

A

Joint pain and functional impairment

35
Q

Most common joints involved in OA

A

Knees, hips, DIP/PIP/1st CMC joint, spine (cervical/lumbar), 1st MTP joints

36
Q

Pathogenesis of OA

A

Involves all the joint tissues (cartilage, bone, ligaments, synovium) due to many factors

37
Q

What happens to the joint in OA?

A

Progressive loss and destruction of cartilage (joint space narrows)
Bony changes to joint: thinking of subchondral bone (bone sclerosis), subchondral cysts, osteophytes (bone spurs)
Synovial inflammation
May see soft tissue components affected

38
Q

What is pathognomonic of OA?

A

Osteophytes (bone spurs)

39
Q

Factors thought to lead to OA

A

Aging, joint injury, obesity, genetics, anatomic factors, females

40
Q

Clinical presentation of OA

A

Joint pain worse with use and relieved by rest
Stiffness is worse after effort (so seen in evening)
If there is morning stiffness, it is less than 30 min

41
Q

Physical findings of OA

A

TTP, reduced ROM, bony enlargement/swelling, joint deformity, joint instability

42
Q

What do the hands look like in OA?

A

Bilateral
Heberdens and Bouchards nodes (classic)
First carpometacarpal joint is squared off

43
Q

What do the knees and hips look like in OA?

A

Knees: bilateral, swelling, joint line tenderness, crepitus, limited ROM
Hips: unilateral, restricted internal ROM, pain around hip/groin, may refer to knee (if you see hip problems on an xray that is advanced disease)

44
Q

What is seen on an Xray in OA?

A

Joint space narrowing, osteophyte fomration, subchondral sclerosis, subchondral cysts

45
Q

Pharmacologic tx of OA

A

Oral and topical NSAIDs used most
Topical capsaicin
Cymbalta (Duloxetine)- SSRI and NE inhibitors
And others

46
Q

When do you do surgery for OA?

A

When they have failed the less invasive modes of therapy

47
Q

Main presentation of polymyalgia rheumatica

A

Proximal aching and stiffness (pelvic girdle, shoulder and neck)
Worse in the morning over an hour because inflammatory

48
Q

Prevalence of PMR

A

Mostly over 50
Peak between 70 and 80
Females
Northern European descent

49
Q

What is PMR associated with?

A

Giant cell (temporal) arteritis

50
Q

What causes the sxs of PMR?

A

Nonerosive synovitis and tenosynovitis

51
Q

Clinical presentation of PMR

A

Recent, discrete change in sx
Bilateral
Shoulder and pelvic girdle pain
Morning stiffness and gel phenomenon (stiffness with inactivity)

52
Q

What is seen on the physical exam with PMR?

A

Limited ROM (common to see limitation of active abduction)
Normal strength but subjective weakness
Synovitis

53
Q

Diagnositc studies in PMR

A

Elevated ESR and/or CRP (ESR often over 50 mm/hr)
May see normocytic anemia
Normal and negative for other tests/antibodies

54
Q

When is there the most rapid resolution of PMR?

A

With low dose glucocorticoids (10-20 mg/day)

55
Q

What is fibromyalgia?

A

Chronic widespread musculoskeletal pain and tenderness often with fatigue, cognitive disturbances etc
More in women (20-50)
Often occurs with RA and SLE

56
Q

Pathophysiology of fibromyalgis

A

Central pain processing (heightened/altered sensation of pain)
Strong genetic predisposition

57
Q

Clinical presentation of fibromyalgia

A

Widespread MSK pain
Fatigue and poor sleep
Cognitive disturbances (fibro fog)
Psychiatric disturbances

58
Q

Other sxs/disorders seen in fibromyalgis

A

Headache, pelvic pain, IBS, interstitial cystitis/painful bladder syndrome, obstructive sleep apnea, restless legs syndrome

59
Q

History seen with fibromyalgia

A

Widespread MSK pain and tenderness (muscles and joints) for over 3 months
Achiness

60
Q

What abnormalities are seen in labs with fibromyalgia?

A

None

61
Q

Pharmacologic tx of fibromyalgia

A

Tricyclic antidepressants (amitriptyline)
Serotonin and NE reuptake inhibitors (SNRIs) like Cymbalta or Savella
Anticonvulsants (Lyrics or Neurontin)
NO OPIOID NARCOTICS

X Clin Med Exam 3 (8 decks)

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